Objective Several studies on the health-related quality of life (HRQL) and imaging scores in patients with chronic rhinosinusitis (CRS) indicated asthma as a comorbidity with a significant impact on subjective and objective outcomes. However, these studies did not adjust the data for other confounders which may interfere with the CRS outcomes. This study aims to evaluate how asthma influences clinical symptoms, imaging scores and HRQL in CRS patients.Methods The study enrolled CRS patients and collected data about asthma status, clinical symptoms, allergic sensitization, computed tomography (CT) and 22-item SinoNasal Outcome questionnaire (SNOT-22). Matching pairs of asthmatic and non-asthmatic CRS patients were defined based on age, gender and nasal polyp presence. The difference between pairs in clinical symptoms, CT and SNOT-22 was then analyzed. The study enrolled mild to moderate asthma patients.Results From 250 CRS patients, 65 (26%) had had asthma. We found 60 CRS asthma and CRS non-asthma pairs based on age, gender and nasal polyp presence. There was no difference in total SNOT-22 score between asthma (46.5) and non-asthma (43.5) CRS groups(p? less then ?0.357). There were more patients with allergy positive medical history in the asthma group (66.1%) when we stratified for CRS phenotypes, gender and age. When comparing the visual analogue scale (VAS) scores for clinical symptoms, smell (p? less then ?0.013) was the only symptom significantly worse in the CRS asthma group. Although there was no difference in Lund-Mackay score, there was a slightly higher osteitis score in the CRS asthma group (5.21 versus 3.45; p= 0.059).Conclusion CRS patients with asthma have significantly worse impairment of smell and taste when compared to non-asthmatic CRS patients. This is the only significant difference which is independent of nasal polyp presence, gender, age and allergy.Background Gastric carcinoma (GC) patients usually present with locally advanced or metastatic disease; therefore treatment aim is mainly palliation. In this study our purpose is to analyze the prognostic values of the sarcopenia index (SI), cachexia index (CIn) and other inflammatory indexes (advanced lung cancer inflammation index [ALI], modified Glasgow Prognostic Score [mGPS], prognostic index [PI], prognostic nutritional index [PNI] and neutrophil-to-lymphocyte ratio [NLR]) in metastatic GC patients.Methods Data from the files of metastatic GC patients, who applied to Medical Oncology outpatient clinic in Marmara University Pendik Education and Research Hospital between January 2011 and June 2016, were retrospectively reviewed. Five hundred seventy patients with gastric cancer were detected. Exclusion criteria were the inability to reach the patient surveys for prognostic index calculations, the presence of additional comorbidities to affect the laboratory parameters, and the absence of metastatic diseasexpensive, practical and beneficial to use in routine clinical practice to determine survival.Boesenbergia rotunda (L.) Mansf. is an edible herb that is commonly used in the cuisine of several Asian countries. Studies have shown that it possesses high bioactivity against a variety of cancer cells. In this study, we investigated the cytotoxic activity of Boesenbergia rotunda rhizomes and some of its constituents on nasopharyngeal carcinoma cells (HK1). MTT assay results showed that the methanolic and hexane extracts of Boesenbergia rotunda decreased HK1 cell viability with IC50 values of 136??g/ml and 66??g/ml, respectively. Cardamonin, a constituent of Boesenbergia rotunda, exhibited the highest cytotoxic activity with an IC50 value of 27?μg/ml. Further studies on cardamonin revealed that it inhibited the migration of HK1 cells, caused G2/M-phase arrest and induced apoptosis. Apoptosis was induced via activating caspase-8 and caspase-3, but independent of caspase-9. https://www.selleckchem.com/products/acetalax-oxyphenisatin-acetate.html This indicated that cardamonin induced extrinsic apoptosis. Western blot analysis further showed that cardamonin caused extrinsic apoptosis, as the expression levels of intrinsic apoptosis-related proteins (Bcl-XL, Bcl-2 and Bax), were not affected. Finally, JC-1 staining of HK1 cells revealed an increase in the mitochondrial membrane potential after treatment, further proving that cardamonin did not induce apoptosis via the intrinsic pathway. These results reflect cardamonin's potential as an anticancer agent.Anticancer drugs, such as Mitomycin C (MMC), can interact with biological molecules and cause genetic damage in normal cells. In this respect, we investigated the potential of chrysin, a flavone known as a potent scavenger of free radicals generated by anticancer agents, to protect mice against MMC-induced genotoxicity. The amount of DNA damage in the liver, kidney and bone marrow cells, in Balb/C mice treated with MMC (6?mg/kg, i.p) and the frequency of chromosomal aberrations indicated the genotoxic effect of MMC. Besides, a significant increase in the activities of antioxidant enzymes (SOD, CAT, GPx, GST) and lipid peroxidation is revealed. On the other hand, we noticed a regression of the genotoxic effect when studying the same parameters in Balb/C mice treated with chrysin (40?mg/kg b. wt., i.p) 24?h prior to MMC (6?mg/kg, i.p) injection. This study concluded that the protective effect of chrysin against genotoxicity of MMC results partly from its antioxidant effect.Brain metastases occur in up to 25-55% of patients with metastatic HER2-positive breast cancer. Standard treatment has high rates of recurrence or progression, limiting survival and quality of life in most patients. Temozolomide (TMZ) is known to penetrate the blood-brain barrier and is US FDA approved for treatment of glioblastoma. Our group has demonstrated that low doses of TMZ administered in a prophylactic, metronomic fashion can significantly prevent development of brain metastases in murine models of breast cancer. Based on these findings, we initiated a secondary-prevention clinical trial with oral TMZ given to HER2-positive breast cancer patients with brain metastases after recent local treatment in combination with T-DM1 for systemic control of disease. Primary end point is freedom from new brain metastases at 1 year. (NCT03190967).